Human infection with swine–origin virus is mostly likely to occur when
people are in close proximity to infected pigs.
The above comment is also in the latest
CDC “Have You Heard” and is also in the “Hopes
and Dreams” category. The data is created by a strong bias in
trH3N2 testing, which is done solely by the CDC and almost exclusively
on samples from cases with a close proximity to swine.

So far this year, the
CDC has not provided any evidence for trH3N2 infection in any swine in
close proximity to the five confirmed trH3N2 cases, and there have been
no reports by any agency on swine infected with the constellation of
genes found in all of the five confirmed 2011 trH3N2 cases. The
above mantra has been repeated so many times that other agencies, such
as the Maine CDC misstated
the history of the 2011 trH3N2 cases, claiming all have been
exposed to swine, which is not true for the Indiana case (2M) who was
exposed to a caretaker with swine exposure. However neither the
caretaker nor the associated swine were symptomatic and none have been
reported to have been infected wit SOIV, trH3N2, or trH3N2 with the
constellation found in the Indiana and Pennsylvania cases.
Moreover, the CDC has classified the Indiana case as limited human to
human transmission. The misstatement in the Maine advisory has
been propagated by various media outlets, as well as ProMED,
which is widely read by media reporters.

The CDC testing for
trH3N2 is dependent on receipt of appropriate samples from state labs,
but identification of trH3N2 samples is problematic because the H3 is
from a seasonal H3N2 infection of swine in the 1990’s.
Consequently, 2010 trH3N2 isolates like A/Pennsylvania/40/2010 were
reported 5 months after infection because of initial designation as
seasonal H3N2. The recent isolate from Maine, A/Maine/06/2011 was
inconclusive
in serotype testing, while more evolved isolates, like
A/Pennsylvania/09/2011 were designated unsubtypables because the sample
was influenza A positve, but H3 negative because it had evolved away
from the original human H3 sequences.

However, the subtyping
data can be unreliable. The four H3 sequences from Indiana and
Pennsylvania were very closely related to each other, but only two were
listed in the sub-typing table and figure in the CDC’s FluView (for
weeks 33 and 34). However, the reporting of these two cases was inconsistent,
appearing in reports for weeks 35 and 36, disappearing win reports for
weeks 37 and 38, reappearing in week 39, and disappearing in week
40. Moreover the week 39 table reported both unsubtypables, while
the figure based on the table only reported the week 33 cases.
These weekly fluctuations for these two samples suggest criteria for
calling samples unsubtypable were in a constent state of flux, and the
other two trH3N2 were not listed in the table or figures for any of the
FluView reports.

In addition to the
variations for the known trH3N2 cases, undercounts are created through
a lack of testing. The majority (67) of the 107 influenza A
positive cases reported for the last
10 weeks of the 2010/2011 season (weeks 30-39), so it is unlikely
that these samples were sent to the CDC, especially since the MMWR
report on the Indiana and Pennsylvania cases requested samples from
cases with swine exposure, which may have led to the identification of
the case in Maine, since he had attended an agricultural fair, and the
sub-typing data was inclusive. The absence of a swine lin would
have probably limited additional testing, which is only done by the
CDC. The absence of the PCR swine H3 from state labs has severely
impacted the detectio of trH3N2 cases, especially those without swine
contact.

Thus, these tests
should be distributed to sate labs, and aggressive testing of influenza
A positive samples should be implemented, regardless of swine exposure.